I had a debate on this in school. Ive researched marijuana intensively and it is very hard to find information on these changes. There has to be some beneficial use to cannabinoids do to their natural release after exercise. There are actually several university studies with (university of Berlin or madrid I think, I did most of my research on pub med and legitimate websites however it was on a school computer and I no longer have pub med access) rats where they had lung cancers induced and then they added cannabinoids. In many of the cases the cancer was slowed and sometimes stoped or reversed.

However there is a serious lack of human trials where marijuana is smoked without the addition of tobacco, skewing the results.

Medical Marijuana doctors in CA warn of decreased testosterone associated with heavy use but that could be partly due to the damage associated by smoking

There are also obesity issues associated with overeating from the munchies. Higher body fat percentage -> lower testosterone...

Hey doc, do you know what kind of effects marijuana has if any on insulin, lepitin, cortisol, testosterone, estrogen, etc?

I am not sure about any of that lol but what i have heard that it is good for weight loss. People say that you get the munchies after you smoke the ganja and you just want to eat eat eat eat! But if you hold off that temptation and not eat after you smoke your metabolism kicks in and i heard you can lose some serious weight. My cousin who smokes weed every single day! Is ripped and skinny as fuh its crazy cause the kid has like bags of skittle sour patch kids and potato chips always in his room munchin on em... and he works out maybe 2-3 times a week.

The purpose of this study was to investigate the effect of chronic uptake of bhang, prepared from the Cannabis sativa, on male reproductive physiology in adult male Parkes strain (P) mice. An attempt was also made to investigate the presence of cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors, and fatty acid amide hydrolase (FAAH) in the testis and to evaluate any changes in it resulting from chronic intake of bhang in mice.METHODS AND RESULTS:

Adult male mice were given bhang (3 or 6 mg/kg body weight/day) orally for 36 consecutive days. Chronic intake of bhang caused regressive changes in the testes and suppressed sperm count, viability and motility. Bhang intake also caused significant decline in circulating testosterone level due to decline in testicular 3β HSD enzyme activity. An immunohistochemical study demonstrated the presence of CB1, CB2 and FAAH in the testis of mice. The present study also showed significant variation in the CB1 and CB2 receptors and FAAH protein levels in testes of mice exposed to bhang. These suppressive effects may be due to inhibitory effect of bhang on pituitary expression of gonadotrophin releasing hormone (GnRH) I receptor protein. Treatment of testes with bhang in vitro significantly decreased testicular luteinizing hormone receptor (LHR) and FAAH expression suggesting direct action of bhang on testicular activity.CONCLUSIONS:

Intraperitoneal injection of cannabis extract at low doses (total doses ranging from 40 mg to 60 mg per mouse) induced adverse effect on testes and oxidative stress. At low doses, there was a significant increase in lipid peroxidation and decrease in testicular lipid content, but the effects were significantly less at higher doses and at the withdrawal of cannabis treatment (recovery dose). There was a marked decrease in antioxidant enzyme profiles (superoxide dismutase, catalase and glutathione peroxidase) and glutathione content at low doses, but these effects were higher at higher dose and at withdrawal of the treatment (recovery effect). Histology revealed significant shrinkage of tubular diameter and detrimental changes in seminiferous epithelium of testis with resulting lowered serum testosterone and pituitary gonadotropins (follicular stimulating [FSH] and luteinizing hormones [LH]) levels at low doses. But at higher doses and particularly at withdrawal of the treatment, regression of various germ cell layers of testes through the revival of testosterone hormone and pituitary gonadotropins (FSH and LH) were observed, indicating that recovery effects on testes became operative possibly through the corrective measure of endogenous testicular antioxidant enzymes profiles and pituitary gonadotropins hormones feedback mechanisms.

The putative role of the endocannabinoid system and the effects of cannabis use in male and female sexual functioning are summarized. The influence of cannabis intake on sexual behavior and arousability appear to be dose-dependent in both men and women, although women are far more consistent in reporting facilitatory effects. Furthermore, evidence from nonhuman species indicate somewhat more beneficial than debilitating effects of cannabinoids on female sexual proceptivity and receptivity while suggesting predominantly detrimental effects on male sexual motivation and erectile functioning. Data from human and nonhuman species converge on the ephemeral nature of THC-induced testosterone decline. However, it is clear that cannabinoid-induced inhibition of male sexual behavior is independent of concurrent declines in testosterone levels. Investigations also reveal a suppression of gonadotropin release by cannabinoids across various species. Historical milestones and promising future directions in the area of cannabinoid and sexuality research are also outlined in this review.
Copyright 2009 Elsevier Inc. All rights reserved.

Aim of the study was to evaluate whether endothelial dysfunction is a marker of erectile dysfunction (ED) in recreational drug abuse. Sixty-four non-consecutive men complaining of ED from at least 3 months were included. All patients underwent detailed history about recreational drug abuse and were then submitted to dynamic penile duplex ultrasound (PDU). According to pharmaco-stimulated peak systolic velocity (PSV) cutoff at 35 cm s(-1), patients were divided into two groups: organic (O; n=30) and non-organic (NO; n=34) ED. All subjects and 7 healthy age-matched subjects as controls, underwent veno-occlusive plethysmography (VOP) for the evaluation of endothelium-dependent dilatation of brachial arteries. Blood pressure, total and free testosterone, prolactin, estradiol, low-density lipoprotein and high-density lipoprotein cholesterol were also evaluated; patients were classified with regard to insulin resistance through the HOMA-IR index. Cannabis smoking was more frequent in O-ED vs NO-ED (78% vs 3%, P<0.001) in the absence of any concomitant risk factor or comorbidity for ED. VOP studies revealed impaired endothelium-dependent vasodilatation in O-ED but not in NO-ED and controls (12+/-6 vs 32+/-4 and 34+/-5 ml min(-1), respectively; P=0.003). Overall patients showed a direct relationship between HOMA-IR and PSV (r(2)=0.47, P<0.0001), which was maintained in men with organic ED (r(2)=0.62, P<0.0001). In cannabis consumers, a direct relationship between HOMA-IR and VOP was also found (r(2)=0.74, P<0.0001). Receiver-operating characteristic (ROC) curve analysis revealed that VOP values below 17.22 ml min(-1) were suggestive for vasculogenic ED. We conclude that early endothelial damage may be induced by chronic cannabis use (and endocannabinoid system activation); insulin resistance may be the hallmark of early endothelial dysfunction and may concur to determine vascular ED in the absence of obesity. Further studies are warranted to establish a direct relationship between cannabis abuse, onset of insulin resistance and development of vascular ED.

The progesterone 17alpha-hydroxylase activity, which is one of the steroidogenic enzymes in rat testis microsomes, was significantly inhibited by crude marijuana extracts from Delta(9)-tetrahydrocannabinolic acid (THCA)- and cannabidiolic acid (CBDA)-strains. Delta(9)-Tetrahydrocannabinol, cannabidiol and cannabinol also inhibited the enzymatic activity with relatively higher concentration (100-1000 microM). Testosterone 6beta- and 16alpha-hydroxylase activities together with androstenedione formation from testosterone in rat liver microsomes were also significantly inhibited by the crude marijuana extracts and the cannabinoids. Crude marijuana extracts (1 and 10 microg/ml) of THCA strain stimulated the proliferation of MCF-7 cells, although the purified cannabinoids (THC, CBD and CBN) did not show significant effects, such as the extract at the concentration of 0.01-1000 nM. These results indicate that there are some metabolic interactions between cannabinoid and steroid metabolism and that the constituents showing estrogen-like activity exist in marijuana.

Department of Anesthesia, College of Medicine, University of Iowa, Iowa City 52242.

Abstract

To investigate possible effects of chronic marijuana use on reproductive and stress hormones, we assayed testosterone, luteinizing hormone, follicle stimulating hormone, prolactin, and cortisol in 93 men and 56 women with a mean (+/- S.E.) age of 23.5 +/- 0.4 years. Hormone values were compared among groups of subjects stratified according to frequency of marijuana use (frequent, moderate and infrequent; N = 27, 18, and 30, respectively) and non-using controls (N = 74). Chronic marijuana use showed no significant effect on hormone concentrations in either men or women.

The object of this study was to establish possible influences of long-term cannabis usage on plasma testosterone levels. The plasma testosterone levels of 66 male Pakistani who for years had smoked cannabis daily or drank cannabis regularly where measured after chronic and acute intake of the drug and compared with a material of 41 normal controls, i.e. persons who did not use cannabis. An evaluation of the results showed that there were no significant differences between the two groups. No influence of long-term cannabis usage on plasma testosterone levels was found. Furthermore we wished to find out wether long-term heroin abuse showed an effect on plasma testosterone levels. The concentrations of testosterone in the plasma of 102 heroin addicts assigned to a Methadone Program were measured and compared with the values of 29 male healthy students as controls. Plasma testosterone levels were found to be significantly decreased in heroin addicts as compared to controls.

Department of Physiology, Southern Illinois University School of Medicine, Carbondale 62901.

Abstract

Male rats exposed to sexually receptive females, exhibit a rapid increase in plasma levels of luteinizing hormone (LH) and prolactin, and concomitant increases in noradrenergic activity in the medial basal hypothalamus (MBH) and median eminence (ME) as well as in dopaminergic activity in the MBH. Delta-9-tetrahydrocannabinol (THC; 5 mg/kg b.wt., PO), the chief psychoactive constituent of marijuana, blocked the MBH and ME noradrenergic response and the dopaminergic response in the MBH in male rats exposed for 20 min to sexually receptive females, and suppressed the expected increases in plasma LH and prolactin levels. Moreover, THC treatment decreased the percentage of animals exhibiting copulatory behavior and increased the latency periods to mount and intromit. These findings indicate that THC interferes with the neuroendocrine and behavioral responses of male rats to the presence of a receptive female.

The main groups of drugs that affect male libido, potency, sperm production, structure and function are summarized and their mechanisms described when known. About 15% of the 200 most commonly prescribed drugs can have adverse effects on male reproduction. Sedatives, tranquilizers, hypnotics, antiandrogens and the common antihypertensive methyldopa can depress libido. Spironoacetone has been reported to impair libido, potency, sperm count and motility, although reversibly. The phenothiazines and tricyclic antidepressants may induce prolactin secretion and consequent gynecomastia. Narcotics and hallucinogens influence male sexual performance. Morphine and methadone decrease LH and testosterone, and increase prolactin. Cannabis, hashish and marijuana initially increase libido and potency, but chronic use causes sexual inversion. Chronic alcoholism also may upset testosterone metabolism, causing testicular atrophy. Cyclophosphamide, used for nephrotic syndrome, and nitrofurans, used as food preservatives, cause direct damage to seminiferous tubules. Synthetic oganochlorine pesticides, especially DDT, have also been reported to damage spermatogenic cells directly, when injected in mice. Steroids such as ACTH, hydrocortisone and dexamethasone may inhibit steroidogenesis in animals.

I could continue to post studies, but you see what I am getting at in terms of Testosterone I hope...the data is simply MIXED. It is possible that different metabolites of THC have different effects that offset one another (and honestly, no one can adequately predict metabolic processing not only from a person-to-person basis, but also a species of plant-to- species of plant basis.

The endocannabinoid system (just talking from a receptor standpoint) is VERY complex (and unfortunately just something well beyond the scope of this thread - as I could focus a dissertation on). I try and remain as objective as is possible here, so I will post data on ALL sides. Please don't suggest that "Dr. Houser suggests I use or I don't use marijuana." I am a pro-choice person, but believe it becomes a problem when it negatively impacts progression through life (not always identified by the user themselves or even those around them - could they have been a better contributer to society? I have no idea!).

I think alcohol is a good example - I mean, I have seen some HIGHLY FUNCTIONAL ALCOHOLICS in medical practice (as I am sure you could believe). At the same time, does that mean they aren't negatively impacting their own physiology...hard to say; some clear alcohol pretty well from the system and you can function with only 15% of your liver in working order due to it's regenerative capacity - which explains why it takes so long for cirrhotic elements to develop. If someone understands the potential exists for a negative effect and still chooses to engage in said activity; who am I to interject per se? I present as objective information as feasibly possible and then its still up to each person to have a sense of personal responsibility in whatever direction they choose. People tend to identify with compounds like these as either ALL evil or ALL good - I say screw the paternalistic view - you don't have to convince someone of your belief per se; you're given a brain for a reason - use it!

Hopefully I was as diplomatic as I could possibly have been to both "sides."

Center for Medicinal Cannabis Research (CMCR) and HIV Neurobehavioral Research Center (HNRC), University of California, San Diego, USA.

Abstract

RATIONALE:

The endocannabinoid system is under active investigation as a pharmacological target for obesity management due to its role in appetite regulation and metabolism. Exogenous cannabinoids such as tetrahydrocannabinol (THC) stimulate appetite and food intake. However, there are no controlled observations directly linking THC to changes of most of the appetite hormones.
OBJECTIVES:

We took the opportunity afforded by a placebo-controlled trial of smoked medicinal cannabis for HIV-associated neuropathic pain to evaluate the effects of THC on the appetite hormones ghrelin, leptin and PYY, as well as on insulin.
METHODS:

In this double-blind cross-over study, each subject was exposed to both active cannabis (THC) and placebo.
RESULTS:

Compared to placebo, cannabis administration was associated with significant increases in plasma levels of ghrelin and leptin, and decreases in PYY, but did not significantly influence insulin levels.
CONCLUSION:

These findings are consistent with modulation of appetite hormones mediated through endogenous cannabinoid receptors, independent of glucose metabolism.

Department of Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96813.

Abstract

Cannabis is the most abused illegal substance in the United States. Alterations in brain function and motor behavior have been reported in chronic cannabis users, but the results have been variable. The current study aimed to determine whether chronic active cannabis use in humans may alter psychomotor function, brain activation, and hypothalamic-pituitary-axis (HPA) function in men and women. Thirty cannabis users (16 men, 14 women, 18-45 years old) and 30 nondrug user controls (16 men, 14 women, 19-44 years old) were evaluated with neuropsychological tests designed to assess motor behavior and with fMRI using a 3 Tesla scanner during a visually paced finger-sequencing task, cued by a flashing checkerboard (at 2 or 4 Hz). Salivary cortisol was measured to assess HPA function. Male, but not female, cannabis users had significantly slower performance on psychomotor speed tests. As a group, cannabis users had greater activation in BA 6 than controls, while controls had greater activation in the visual area BA 17 than cannabis users. Cannabis users also had higher salivary cortisol levels than controls (p = 0.002). Chronic active cannabis use is associated with slower and less efficient psychomotor function, especially in male users, as indicated by a shift from regions involved with automated visually guided responses to more executive or attentional control areas. The greater but altered brain activities may be mediated by the higher cortisol levels in the cannabis users, which in turn may lead to less efficient visual-motor function.

Background: The endocannabinoid system modulates the hypothalamic-pituitary-adrenal (HPA) axis, but the effect of cannabinoid type 1 (CB1) receptor antagonism following chronic CB1 receptor stimulation in humans is unknown. Objectives: To evaluate effects of the CB1 receptor antagonist rimonabant on the HPA axis in cannabis-dependent individuals. Methods: Fourteen daily cannabis smokers received increasingly frequent 20 mg oral Δ9-tetrahydrocannabinol (THC) doses (60-120 mg/day) over 8 days to standardize cannabis tolerance. Concurrent with the last THC dose, double-blind placebo or rimonabant (20 or 40 mg) was administered. Cannabinoid, rimonabant, and cortisol plasma concentrations were measured 1.5 hours prior to rimonabant administration and 2.0, 5.5, and 12.5 hours post-dose. Results: Ten participants completed before premature study termination due to rimonabant's withdrawal from development. Five participants received 20 mg, three received 40 mg, and two placebo. There was a significant positive association between rimonabant concentration and change in cortisol concentration from baseline (r = .53, p < .01). There also was a borderline significant association between rimonabant dose and cortisol concentrations when the dose-by-time interaction was included. Four of eight participants receiving rimonabant (none of two receiving placebo) had greater cortisol concentrations 2 hours after dosing (at 11:30) than at 08:00, while normal diurnal variation should have peak concentrations at 08:00. Conclusion: Rimonabant 20 or 40 mg did not significantly increase plasma cortisol concentrations, consistent with an absence of antagonist-elicited cannabis withdrawal. Scientific Significance: Rimonabant doses >40 mg might elicit cortisol changes, confirming a role for CB1 receptors in modulating the HPA axis in humans.

PMID:21797816[PubMed - as supplied by publisher]

You do have to appreciate that there are differences between Rimonobant and what you'd receive on the street though...(just make sure you understand this...).

And I can go on and on with posting studies and offering interjection, but I think we should stop and summarize on the effects of the hormones that were listed in post #1.

1. Testosterone: Mixed - most current studies suggest LOWERING of T levels, but studies through the 90s did NOT suggest such a pattern - they SAID NO CHANGE, studies before the 90s also said LOWERING - lot of reasons likely behind the discrepency (populations studied; different metabolic processing / metabolites; and so on...). Also a significant bias on the part of the researchers likely explains some of the trends.

And I can go on and on with posting studies and offering interjection, but I think we should stop and summarize on the effects of the hormones that were listed in post #1.

1. Testosterone: Mixed - most current studies suggest LOWERING of T levels, but studies through the 90s did NOT suggest such a pattern - they SAID NO CHANGE, studies before the 90s also said LOWERING - lot of reasons likely behind the discrepency (populations studied; different metabolic processing / metabolites; and so on...). Also a significant bias on the part of the researchers likely explains some of the trends.

4. Cortisol: RAISES (again pretty unanimous); this one is interesting and NOT surprising at all given the appetite control data. Please don't view cortisol elevations as inherently BAD all the time.

D_

Thanks for posting up all those studies. Now, when I argue with my friends that using chronic chronically (see what i just did lol) may have a negative impact, depending on the individual, I can actually have a good set of references that I can look up with a few clicks. I knew that marijuana does raise cortisol, but what I'm wondering is how much does it raise it if one were to use marijuana say 5x a week compared to once a week, and ONLY after workouts; seeing as how cortisol is spiked naturally after workouts.

I think for the most part those studies do not reflect the matter in which we are after...and that is how it effects young-middle aged males, who engage in mild-high level activities, 3-5x a week. I think for most of us on this board, that would describe us pretty well. I'd like to see a study on those factors and see what happens with the hormone panel then. I think there would be a significant difference as far as negative effects go. Of course it would be nice if all volunteers would only be allowed to use a certain type of supplement(s) too because let's face it, someone that's using chronic on a cycle is less likely to experience low test levels than someone who isn't; but who knows I may be completely wrong due to the changes in the HPTA from both kinds of substances (PHs/DS and marijuana). Which is why it is absolutely critical for all volunteers to be on the same exact protocol to get a definitive answer, and to, of course, have a control group.

But seeing as how I don't expect that study to ever be performed in the U.S. any time soon, I guess we'll all have to just get our own bloods done and see what happens, heh.

Oh and btw, I don't have anything against marijuana. Like mr.cooper69 said, a lot of people like to create the problems marijuana is blamed for, and I have to say, I completely agree. And like we say on this board, too much of a good thing can be a bad thing or rather, too much of anything can be a bad thing.

Thanks for posting up all those studies. Now, when I argue with my friends that using chronic chronically (see what i just did lol) may have a negative impact, depending on the individual, I can actually have a good set of references that I can look up with a few clicks. I knew that marijuana does raise cortisol, but what I'm wondering is how much does it raise it if one were to use marijuana say 5x a week compared to once a week, and ONLY after workouts; seeing as how cortisol is spiked naturally after workouts.

I think for the most part those studies do not reflect the matter in which we are after...and that is how it effects young-middle aged males, who engage in mild-high level activities, 3-5x a week. I think for most of us on this board, that would describe us pretty well. I'd like to see a study on those factors and see what happens with the hormone panel then. I think there would be a significant difference as far as negative effects go. Of course it would be nice if all volunteers would only be allowed to use a certain type of supplement(s) too because let's face it, someone that's using chronic on a cycle is less likely to experience low test levels than someone who isn't; but who knows I may be completely wrong due to the changes in the HPTA from both kinds of substances (PHs/DS and marijuana). Which is why it is absolutely critical for all volunteers to be on the same exact protocol to get a definitive answer, and to, of course, have a control group.

But seeing as how I don't expect that study to ever be performed in the U.S. any time soon, I guess we'll all have to just get our own bloods done and see what happens, heh.

Oh and btw, I don't have anything against marijuana. Like mr.cooper69 said, a lot of people like to create the problems marijuana is blamed for, and I have to say, I completely agree. And like we say on this board, too much of a good thing can be a bad thing or rather, too much of anything can be a bad thing.